ArticleAmerican journal of physiology. Renal physiology2013
Molecular evidence for a role for K(+)-Cl(-) cotransporters in the kidney.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Exploring the Role of the SLC12A Cation-Coupled Chloride Cotransporters in the Cardiovascular System.Cells · 2026Review
- KCC3 is not required for the distal convoluted tubule response to reduced dietary potassium intake.American journal of physiology. Renal physiology · 2025Article
- A brief history of the cortical thick ascending limb: a systems-biology perspective.American journal of physiology. Renal physiology · 2025Review
- Role of calcineurin in regulating renal potassium (KActa physiologica (Oxford, England) · 2024Review
- The K-Cl cotransporter-3 in the mammalian kidney.Current opinion in nephrology and hypertension · 2023Review
- Review
- SGLT2 inhibitors, intrarenal hypoxia and the diabetic kidney: insights into pathophysiological concepts and current evidence.Archives of medical sciences. Atherosclerotic diseases · 2023Article
- KCC3a, a Strong Candidate Pathway for KFrontiers in cell and developmental biology · 2022Article
- DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation.iScience · 2021Article
- SIRT7 modulates the stability and activity of the renal K-Cl cotransporter KCC4 through deacetylation.EMBO reports · 2021Article
- WNK4 kinase: from structure to physiology.American journal of physiology. Renal physiology · 2021Review
- Metabolic acidosis and hyperkalemia differentially regulate cation HCN3 channel in the rat nephron.Journal of molecular histology · 2020Article
- Opioid Preconditioning Modulates Repair Responses to Prevent Renal Ischemia-Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Review
- Coordinate adaptations of skeletal muscle and kidney to maintain extracellular [KAmerican journal of physiology. Cell physiology · 2020Article
- The Molecular Genetics of Gordon Syndrome.Genes · 2019Review
- Physiological roles and molecular mechanisms of KThe Journal of physiology · 2019Review
- SLC12A7 alters adrenocortical carcinoma cell adhesion properties to promote an aggressive invasive behavior.Cell communication and signaling : CCS · 2018Article
- Underdominant KCC3b R31I association with blood sodium concentration in domestic sheep suggests role in oligomer function.Animal genetics · 2017Article
- WNK signalling pathways in blood pressure regulation.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
K(+)-Cl(-) cotransporter (KCC) isoforms 3 (KCC3) and 4 (KCC4) are expressed at the basolateral membrane of proximal convoluted tubule cells, and KCC4 is present in the basolateral membrane of the thick ascending loop of Henle's limb and α-intercalated cells of the collecting duct. Little is known, however, about the physiological roles of these transporters in the kidney. We evaluated KCC3 and KCC4 mRNA and protein expression levels and intrarenal distribution in male Wistar rats or C57 mice under five experimental conditions: hyperglycemia after a single dose of streptozotocin, a low-salt diet, metabolic acidosis induced by ammonium chloride in drinking water, and low- or high-K(+) diets. Both KCC3 mRNA and protein expression were increased during hyperglycemia in the renal cortex and at the basolateral membrane of proximal tubule cells but not with a low-salt diet or acidosis. In contrast, KCC4 protein expression was increased by a low-sodium diet in the whole kidney and by metabolic acidosis in the renal outer medulla, specifically at the basolateral membrane of α-intercalated cells. The increased protein expression of KCC4 by a low-salt diet was also observed in WNK4 knockout mice, suggesting that upregulation of KCC4 in these circumstances is not WNK4 dependent. No change in KCC3 or KCC4 protein expression was observed under low- or high-K(+) diets. Our data are consistent with a role for KCC3 in the proximal tubule glucose reabsorption mechanism and for KCC4 in salt reabsorption of the thick ascending loop of Henle's loop and acid secretion of the collecting duct.
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Registered trials
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